Hyperglycemia in the reperfusion period hampers recovery from cerebral ischemia.
Glucose treatment prior to cerebral ischemia is followed by similar metabolic and hemodynamic recovery (Siemkowicz & Gjedde 1980), and normalisation of brain extracellular ions (Siemkowicz & Hansen 1981). In view of this, the present study investigated whether post-ischemic hyperglycemia influenced recovery from cerebral ischemia. In rats which received 50% glucose during a 10 min period of cerebral ischemia, and which had a plasma glucose level of 28.5 mM after 10 min of recirculation, recovery was inferior to that of rats receiving either 8% NaCl or 0.9% NaCl (and hence the rats were normoglycemic). Furthermore, rats which had been rendered hyperglycemic (39 mM) prior to ischemia, and which had plasma glucose lowered to 15 mM by insulin treatment during ischemia, did not recover and died within 4 days. Conversely, rats with somewhat lower preischemic hyperglycemia (28 mM), and which had plasma glucose lowered to 12 mM by insulin treatment during ischemia, recovered as well as the normoglycemic rats. In conclusion, preischemic and postischemic hyperglycemia is detrimental to recovery from cerebral ischemia.
D000818:Animals; D002545:Brain Ischemia / Q000097:blood / Q000150:complications*; D002245:Carbon Dioxide / Q000097:blood; D005947:Glucose / Q000009:adverse effects; D006323:Heart Arrest / Q000628:therapy; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000150:complications*; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D010100:Oxygen / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D002245:Carbon Dioxide; D005947:Glucose; D010100:Oxygen